Researchers at Duke University Medical Center
have demonstrated for the first time what happens inside a cell when it
is deprived of the essential nutrient iron. Iron is found abundantly in
red meats, shellfish dried fruits, whole grains, spinach, seeds and
other foods.
Their study in yeast cells demonstrated that iron-starved cells
preserve the little iron they possess by shutting down the major iron
users in order to maintain the cell's essential functions, said Dennis
J. Thiele, Ph.D., professor of Pharmacology and Cancer Biology at Duke.
He said their discovery could aid in the diagnosis and ultimately the
treatment of serious disorders caused by low iron levels.
Results of his study, funded by the National Institutes of Health, are
published in the Jan. 14, 2005, issue of the journal Cell.

Iron deficiency is the most prevalent and severe nutritional disorder
world wide, affecting more than 2 billion people. The most widely
recognized symptom is anemia, in which too few red blood cells are
produced, and the body is deprived of oxygen needed for energy
metabolism. Iron deficiency causes wide-ranging symptoms from fatigue,
weakness and cognitive deficits to serious heart complications and
developmental disorders. Iron deficiency also contributes to the
pathology of hereditary blood disorders, Parkinson's disease and
certain cancers and develops during a number of chronic diseases, the
researchers said.
Until now, however, a cell's response to iron deprivation was poorly
understood. In the Duke study, Thiele and his Duke colleagues at the
Sarah W. Stedman Nutrition and Metabolism Center demonstrated that the
activity of more than 80 different genes was dramatically reduced in
response to iron deprivation. The function of many of these genes is
unknown, meaning that side effects from iron deprivation may go
unattributed to their root cause. Other genes affected by iron
starvation are known to be vital in generating energy, copying the
cell's genetic code and
protecting the cell from free radicals and
aging, said Thiele.
"We discovered that iron deprivation actually reprograms the metabolism
of the entire cell," said Thiele. "Literally hundreds of proteins
require iron to carry out their proper function, so without this
nutrient, there is a complete reorganization of how cellular processes
occur."
The cellular player responsible for the metabolic reprogramming is a
protein called Cth2. Thiele's team found that iron-deprived cells
overproduce Cth2. This protein binds to the gene expression machinery
of more than 80 different genes and targets these molecules, called
messenger RNA, to be destroyed or degraded. Without messenger RNA, a
gene cannot translate its genetic code into proteins that carry out its
intended functions.
Thiele said the same scenario may occur in human cells, as well, to an
even greater degree. His study was conducted in yeast cells because
their genome is remarkably similar to that of a human cell. In fact,
the Cth2 protein in yeast is quite similar to a family of three
proteins in humans. When the human proteins are substituted in place of
Cth2 in yeast, they actually assume its function in yeast cells, said
Thiele.
"Yeast cells illuminate for us what to look for in human cells," said
Thiele. "Current diagnostic markers for iron deficiency aren't very
sensitive, unless the deficiency is severe. Pinpointing the genes
affected by iron deprivation should provide us with a genetic
fingerprint of what patients with varying levels of iron deprivation
look like."
A patient's blood could easily be tested for specific diagnostic
markers that would indicate his level of iron deprivation, he said.
With diagnostic markers in place, physicians could translate the
severity of the disease into the appropriate treatment.
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